Bacterial persisters refer to a dormant sub-population of cells tolerant to antibiotic treatment and are considered an important source of chronic and recurrent infection. Bacterial persistence is distinguished from antibiotic resistance by the fact that persisters are not genetically different from antibiotic susceptible cells. Instead, persistence results from phenotypic population heterogeneity within an isogenic population. Viewed as part of an epigenetic survival strategy, persisters forfeit rapid growth in order to gain tolerance to diverse stresses including antibiotics. Genetic studies have uncovered a number of cellular phenomena involved in bacterial persistence, including toxin-antitoxin modules and the stringent response. In addition, glycerol, glyoxylate, and phosphate metabolism have been found to affect persistence, indicating that the cellular metabolic state plays a crucial role in the persister phenotype. Genetic studies have also indicated a role for the DNA damage response in the formation of persisters, indicating that persistence may be, in part, inducible. While these advances have expanded our understanding of persister formation they have not addressed how to eliminate bacterial persisters.